Please do I'm looking forward to it.
Thank you for taking the time to reply... First of all I will apologize for advising Tren in a first cycle, that is NOT what we do here, we always advise a single compound Test only for any first cycle. I had clearly missed read the OP...!! (I too am on several private member boards, writing multiple replies at the same time)...
Blood levels should dictate choice on any ancillaries, IF NEEDED..!!
As this is a harm reduction forum we don't advise polypharmacy for conditions you don't have, just because..!! (AI's, D2 agonists)
hCG is sometimes recommended on long blasts for general healthier living, its not needed on a short, low dose, test only cycle...
PCT:
As you approach the start of PCT, as your steroids dissipate you introduce an Aromatase Inhibitor. You do this to reduce the amount of estrogen conversion that takes place.
Your externally administered testosterone will drop to nothing and you will not be producing testosterone as you start PCT. So you want to make sure that you have reduced estrogen as well.
This is just going into PCT. You want to create a situation where both estrogen and testosterone will rise together. So the AI of your choice should be used in the last 2 weeks of the cycle and immediately discontinued at the start of PCT.
The choice of SERM and duration may vary but PCT should always start with Clomid. You do not need a huge dose in the first few days.
Here is what to do:
Start with Clomid for three weeks and reduce the dosage and overlap it with Nolva in week four. Dose Nolva for 3 weeks thereafter.
After 7 weeks in the last day of Nolva introduce an AI and run that by itself for three or four days.
Thats about it. PCTs as you can see are very long. But they are designed to recover from 6 month cycles. PCT is about as long as the cycle.
Then stay off and learn to be natural again for another 6 months or more.
In my opinion this approach can allowed you to fully recover after years of experimentation.
Addendum
Another thing I forgot to mention is don't wait for the steroid ester to completely clear before starting Clomid. Start w/ moderate dosed Clomid EOD or lower dose ED during the time wait for longer esters to clear.
This is relevant for something like Cypionate.... so during the 16 days it takes to clear dose Clomid.
A SERM is not a SERM is not a SERM.
Clomid does more then act as an anti-estrogen in certain tissues. In the pituitary it acts as an estrogen, sensitizing pituitary cells to the actions of gonadotropin-releasing hormone (GnRH). This stimulates release of FSH & LH. Enclomid the active anti-estrogenic component of Clomid is as effective as Clomid in this regard.
Tamoxifen (an anti-estrogen) is completely ineffective.
Clomid mediates the positive effect at the estrogen receptor.
Both Clomid and tamoxifen are almost equally effective at binding to the pituitary estrogen receptor. As noted Tamoxifen has no estrogen mediated effect in terms of an ability to increase GnRH-stimulated release of FSH & LH. What it does is just occupy the receptors...or block them so that E2 or Clomid can not have a positive influence.
That isn't what we want in the first few weeks of PCT. That is why not to use Tamoxifen in those early weeks.
Here is one of several studies demonstrating what I refer to:
Disparate effect of clomiphene and tamoxifen on pituitary gonadotropin release in vitro, E. Y. Adashi, A. J. Hsueh, T. H. Bambino and S. S. Yen,AJP - Endocrinology and Metabolism, Vol 240, Issue 2 125-E130
The direct effects of clomiphene citrate (Clomid), tamoxifen, and estradiol (E2) on the gonadotropin-releasing hormone (GnRH)-stimulated release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were studied in cultured anterior pituitary cells obtained from adult ovariectomized rats. Treatment of pituitary cells with Clomid or enclomid (10(- M) in vitro for 2 days resulted in a marked sensitization of the gonadotroph to GnRH as reflected by a 6.5-fold decrease in the ED50 of GnRH in terms of LH release from 2.2 x 10(-9) M in untreated cells to 3.6 x 10(-10) M.
Treatment with E2 or Clomid also increased the sensitivity of the gonadotroph to GnRH in terms of FSH release by 4.3- and 3.3-fold respectively.
Tamoxifen, a related antiestrogen, comparable to Clomid in terms of its ability to compete with E2 for pituitary estrogen receptors, was without effect on the GnRH-stimulated LH release at a concentration of 10(-7) M. Furthermore, tamoxifen, unlike Clomid, caused an apparent but not statistically significant inhibition of the sensitizing effect of E2 on the GnRH-stimulated release of LH.
Our findings suggest that Clomid and its Enclomid isomer, unlike tamoxifen, exert a direct estrogenic rather than an antiestrogenic effect on cultured pituitary cells by enhancing the GnRH-stimulated release of gonadotropin
PROLACTIN AND GYNO?
Although prolactin receptors have been demonstrated in breast tissue, including gynecomastia [1], hyperprolactinemia probably plays an indirect role in gynecomastia by causing central hypogonadism. Most men with gynecomastia do not have elevated serum prolactin levels, and not all men with hyperprolactinemia develop gynecomastia. Nevertheless, it has been shown in cultured breast cancer cells that prolactin and sex steroid receptors (especially the progesterone receptor [PgR]) may be coexpressed and may cross-regulate each other?s expression [2,3]; acute prolactin treatment produced an increase in PgR and a decrease in AR content. If this were to occur in the breast tissue of hyperprolactinemic men, the resulting increase in PgR expression and decrease in AR expression could promote breast tissue growth and result in gynecomastia.
[1] Gill S, Peston D, Vonderhaar BK, et al. Expression of prolactin receptors in normal, benign, and malignant breast tissue: an immunohistological study. J Clin Pathol 2001;54:956?60.
[2] Ormandy CJ, Hall RE, Manning DL, et al. Coexpression and cross-regulation of the prolactin and sex steroid hormone receptors in breast cancer. J Clin Endocrinol Metab 1997;82(11): 3692?9.
[3] Gutzman JH, Miller KK, Schuler LA. Endogenous human prolactin and not exogenous human prolactin induces estrogen receptor a and prolactin receptor expression and increases estrogen responsiveness in breast cancer cells. J Steroid Biochem Mol Biol 2004;88:69?77. from: Endocrinol Metab Clin N Am (2007) 36: 497?519
While prolactin and progestins on their own don't seem to cause gyno, is it possible that something similar to the post-pregnancy lactation in women could happen in men taking progestational androgens? In this case it might be that increased E and progestational signaling (if you're on a suppressive compound that also acts on the progesterone receptor) causes gyno formation (and increased prolactin levels), and then when you stop the compound and go into PCT (loss of E and progestational signaling), lactation is possible.
In the belief that certain anabolic steroids increase prolactin levels as well as act as agonists at the progesterone receptor, some have advocated the use of antiprolactin agents, like bromocriptine, or progesterone receptor blockers like RU-486 to treat AAS related gynecomastia, in lieu of more traditional drugs like tamoxifen. In truth, the etiology of gynecomastia is unknown and a number of agents including estrogens, progestins, GH, IGF-1, and prolactin may be involved. However, most authorities believe that a decreased (T+DHT)/E ratio is central to the development of gyno, and that blocking the effects of estrogen, or increasing T + DHT levels, is central to ameliorating the problem.
Regarding prolactin, androgens decrease prolactin levels whereas estrogens increase prolactin. Non-aromatizing androgens have never been shown to elevate prolactin levels in humans, but testosterone has, due to its aromatization to estradiol. Prolactin secreting tumors, or prolactinomas, are often associated with gyno. But in these cases the prolactin is believed to induce gyno by suppressing testosterone production: "Prolactinomas that are sufficiently large to cause gynecomastia do so as a result of impairment of gonadotropin secretion and secondary hypogonadism". However, this is a moot issue in AAS users whose gonadotropin secretion is already blunted. According to research, prolactin may have a direct stimulatory effect on mammary tissue development, but only in the presence of high estrogen levels. The presence of mild hyperprolactinaemia is therefore not uncommon in patients with estrogen excess. Significant primary hyperprolactinaemia, on the other hand, may directly stimulate epithelial cell proliferation in an estrogen-primed breast, causing epithelial cell proliferation and gynaecomastia.
So rather than focusing solely on lowering prolactin levels which may be elevated in users of aromatizing androgens, attacking estrogen should be the first line of action.
Progesterone acts in concert with estrogen to promote breast development, and at least part of any role played by synthetic progestins may be to stimulate IGF-1 production in the breast. But again, blocking the action of progesterone or synthetic progestins is not practical. Specific progesterone receptor antagonists like RU-486 block not only the progesterone receptor, but the androgen receptor as well, and have actually been associated with the development of gynecomastia. In any case, progesterone is thought to act on the breast to enhance the effects of estrogen so once again, attacking estrogen is the easiest and most logical approach.
DHT is thought to act as an aromatase inhibitor and perhaps compete directly with estrogen for binding at the estrogen receptor. DHT has been used in several case reports and controlled trials to successfully treat gynecomastia. So perhaps a viable strategy would be to combine DHT gel with tamoxifen. I would recommend tamoxifen rather than an aromatase inhibitor due to the simple fact that tamoxifen has been widely used in numerous controlled studies to succesfully treat gynecomastia, whereas the evidence to support the efficacy of aromatase inhibitors is scanty at best.
Conclusions:
It seems that all the problems that come with increased progestational activity may require high estrogen to become really noticable...so if you can stop the estrogen (on cycle or during the "rebound"), you should have a good chance of avoiding the progestational sides...that's my theory from my reading, anyway.
And finally, prolactin does NOT cause gyno (well, only in extremely rare cases) in most PH/DS/AAS users. It can cause lactation if gyno (generally caused by low T/E ratio, i.e. low T, high E; increased progestational activity is also involved) has progressed to the point where the ductal systems are more developed and prolactin levels have risen enough to trigger lactation. Increased prolactin and subsequent lactation is a side effect of gyno, not a cause.
Androgens overall decrease prolactin. Gyno has always and still is treated solely with anti-estrogen therapy (barring surgery once it gets too big and androgen therapy if the cause is hypogonadism) with no research being done into newer or better ways of treatment. This lends further credence that neither progestins nor prolactin plays any role in gyno in the absence of estrogen, and that standard anti-estrogen therapy (preferably at the receptor to avoid direct drug/ER interactions) should cause gyno to regress in any and all cases.
50+ years of research and countless blood tests have always shown androgens to decrease prolactin levels, with no account ever of androgens having a positive effect on prolactin of prolactin signalling in healthy tissue in the absence of estrogen.
Weidenbach et al (1980) performed a study in castrated and adrenalectomized rats. These rats showed a severe drop in prolactin levels. Treatment with testosterone did not affect prolactin, but treatment with estradiol drastically increased prolactin. The reason for the drop in prolactin in these rats was therefore likely due to the removal of estrogen-producing organs, clearly demonstrating the estrogen-dependency of prolactin release.
Progesterone in the breast, is anti-proliferative, especially in the presence of androgen. It counters gyno.
Lowering Prolactin can potentially lead to among others: reduced testosterone, reduced sperm counts and reduced immunity. Quit messing with your endocrine system for no reason. Keep your prolactin at NORMAL levels and stop using things like Bromocriptine and L-Dopa just "because"
